1. Avian embryo myoblasts do not bind beta-adrenergic antagonists or respond to agonists although they have adenylate cyclase activity. Coincident with fusion to form myotubes, the muscle cells acquire beta-receptors which become functionally coupled to adenylate cyclase. 2. Colchicine, which disrupts microtubules, causes cells to become more responsive to stimulators of adenylate cyclase. Agents which promote microtubule assembly reduce cellular responsiveness. Prolonged exposure of cells to beta-agonists results in desensitization (loss of hormone response), which can be blocked by colchicine. 3. Accumulation of cyclic AMP does not occur in cells treated with cholera toxin for 24 hrs. at or below 15 degrees C whereas accumulation occurs within 35 min. in cells incubated at 37 degrees C. When briefly exposed (20 or 30 min.) at 37 degrees C to toxin and then shifted to 15 degrees C, the cells accumulate cyclic AMP. If exposed for only 10 min., the cells do not respond to the toxin. Antitoxin blocks activation of adenylate cyclase in cells preincubated with toxin at 15 degrees C but not at 37 degrees C. Thus, cholera toxin action appears to involve a time- and temperature-dependent transmembrane event.